Congestive heart failure (CHF) is a highly debilitating and progressive illness that afflicts tens of millions of people worldwide. In the United States, over 4.8 million people currently suffer from this condition and it is estimated that CHF will ultimately affect one in every five Americans. With over 400,000 new cases diagnosed each year in the United States alone, CHF is a rapidly growing public health problem that has proven difficult to treat. Current pharmacologic therapies can relieve symptoms in most patients but do not appreciably stem the course of the disease. Indeed, despite optimal pharmacotherapy and outpatient management, median survival times following initial diagnosis are alarmingly brief—just 1.7 years in men and 3.2 years in women. At present, heart transplantation remains the most effective treatment, but a small donor pool and the serious side effects of immunosuppressive drugs limit this approach. Mechanical circulatory support with a left ventricular assist device (VAD) has been shown to reverse the physiologic effects of severe congestive heart failure and improve both survival and quality of life when compared to medical therapy. In short-term use, as in bridge to cardiac transplantation, this approach has been particularly effective. When intended for permanent support, however, VAD technology has been plagued by problems associated with the complexities of extracorporeal power delivery and thrombolic complications associated with artificial blood contacting surfaces. An alternate approach that allows for a biologically-powered form of mechanical circulatory support devoid of blood-contacting surfaces would therefore be a major advance in the treatment of CHF.
The present invention is related to a broad family of commercial cardiac assist devices the vast majority of which draw blood directly from the heart and pump it back to the systemic circulation by mechanical means. This typically involves using either a blood-borne impeller or a compressible blood sac, both of which remain in intimate contact with the blood being pumped. As a consequence, thromboembolic events, the need for anticoagulation, hemolysis, immune reactions and infections all contribute to the morbidity and mortality of patients supported by these devices. Other more experimental devices avoid direct contact with the blood by using the heart itself as the blood sac. These various “cardiac compression” devices (Anstadt cup; CardioSupport system; HeartPatch; AbioBooster) are similar to the disclosed technology only insofar as they seek to improve cardiac output by manipulating the external structures of the heart. Their mechanism of action, however, is significantly different.
As mentioned above, the existing technology is embodied in several experimental devices designed to achieve direct cardiac compression. These various devices are described in the following publications:                Huang Y, Gallagher G, Plekhanov S, Morita S, Brady P W, Hunyor S N. HeartPatch implanted direct cardiac compression: effect on coronary flow and flow patterns in acute heart failure sheep. ASAIO J. 2003 May-June; 49(3):309-13.        Oz M C, Artrip J H, Burkhoff D. Direct cardiac compression devices. J Heart Lung Transplant. 2000 October; 21(10):1049-55. Review.        Kavarana M N, Helman D N, Williams M R, Barbone A, Sanchez J A, Rose E A, Oz M C, Milbocker M, Kung R T. Circulatory support with a direct cardiac compression device: a less invasive approach with the AbioBooster device. J Thorac Cardiovasc Surg. 2001 October; 122(4):786-7.        Williams M R, Artrip J H. Direct cardiac compression for cardiogenic shock with the CardioSupport system. Ann Thorac Surg. 2001 March; 71(3 Suppl):S188-9.        Lowe J E, Anstadt M P, Van Trigt P, Smith P K, Hendry P J, Plunkett M D, Anstadt G L. First successful bridge to cardiac transplantation using direct mechanical ventricular actuation. Ann Thorac Surg. 1991 December; 52(6):1237-43; discussion 1243-5.        